Craniocerebral Trauma
If early diagnosis of craniocerebral injury is not achieved, patient survival and prognosis are poor. Hypoxemia and hypotension can increase mortality in patients with craniocerebral injury.
The following conditions are potentially dangerous, but difficult to diagnose and treat in primary care. It is important to treat to the best of your experience and condition. Classify and treat the casualty according to the injury.
Acute epidural injury – Basic signs.
Change in consciousness to coma and rapid deterioration ;
Bleeding from the middle meningeal artery with rapid increase in intracranial pressure;
contralateral hemiparesis with fixed ipsilateral pupil.
Acute subdural hematoma – clot in the subdural space with severe contusion of local brain tissue. The cause is a torn bridging vein between the cortex and the dura mater.
Treatment is surgical and decompression by drilling as soon as possible
The following cases should be treated conservatively, as surgery is unlikely to improve the outcome at this time
skull base fracture – bruised eyelids (panda eyes) or mastoid bruises (Battle’s sign), cerebrospinal fluid leak in the ear and nose;
Cerebral contusion – transient changes in consciousness;
Depressed skull fracture – broken pieces of skull can puncture the dura and brain tissue.
Intracerebral hematoma-mostly seen after an acute injury or secondary to a cerebral contusion.
The most common errors in the diagnosis and resuscitation of craniocerebral injury are
Failure to perform initial resuscitation in a timely manner and failure to prioritize;
Failure to identify the underlying cranial injury;
Failure to perform a basic neurological examination of the patient;
Failure to re-examine the patient if the condition deteriorates;
Management of craniocerebral injury
Once the airway, breathing, and circulation (if cervical braking is available) are stabilized, the patient’s neurologic status must be monitored and documented in addition to the patient’s vital sign parameters. A Glasgow coma score can be performed:
Eye opening response score Verbal response score Motor response score score
Automatic eye opening 4 Correct response 5 Movements as instructed 6
Eye opening on call 3 Wrong answer 4 Stinging can be localized 5
Opens eyes with sting 2 Nonsense talk 3 Able to avoid sting 4
Does not open eyes 1 Can only articulate 2 Hyperflexion response 3
Cannot speak 1 Hyperextension reaction 2
Inability to move 1
A GCS score of ≤8 indicates severe cranial injury;
GCS 9-12 indicates moderate cranial injury;
GCS 13-15 points indicate mild craniocerebral injury.
The cause of worsening craniocerebral injury may be active bleeding.
Unequal or dilated pupils on both sides indicate elevated intracranial pressure.
Note the three main signs of increased intracranial pressure: headache; vomiting; and optic nerve papillary edema.
In adults with craniocerebral injury, damage to the head or brain tissue is never a direct cause of hypotension.
Sedation should be avoided in patients with craniocerebral injury. This is because sedation not only interferes with the determination of the state of consciousness, but can also trigger hypercapnia (sedation can cause slowed breathing and lead to CO2 retention).
Cushing’s reaction is a specific response to a sudden rise in intracranial pressure. It indicates an advanced stage of the disease and a poor prognosis. The clinical manifestations include: slow pulse, slow respiration, and high blood pressure (two slow and one high).
The basic management options for severe craniocerebral injury include
Endotracheal intubation, mechanical ventilation, and hyperventilation (PCO2 at 4.5-5 Kpa). This will temporarily reduce intracranial blood volume and reduce intracranial hypertension;
Sedation and, if necessary, inotropes;
Appropriate fluid supplementation, but not excessive, along with diuretics;
Elevation of the head by 20%;
Prevention of elevated body temperature.
Spinal cord injury
The incidence of nerve injury in patients with multiple injuries is much higher than expected. The most common injuries include injury to the nerves innervating the fingers, injury to the brachial plexus, and injury to the spinal cord.
Perform an initial examination to make a determination of the patient’s underlying condition; ABCDE.
The patient with a spinal cord injury should be examined in a neutral position (no flexion, extension, or rotation) without any spinal motion. In such patients: axial turning, appropriate braking (linear braking, wearing a neck brace, sandbag), and neutral position during transport.
If there is a vertebral injury (which may mask spinal cord injury), note: local tenderness, spinal deformity and posterior “step” injury, edema (swelling);
Clinical manifestations of cervical spine injury.
dyspnea (diaphragm-based breathing – check for paradoxical breathing), hypotonia, loss of reflexes (check rectal sphincter), hypotension with bradycardia (but no hypovolemia)
Cervical spine: If available, all patients suspected of having cervical spine injury should have anteroposterior and lateral cervical spine X-rays to clearly demonstrate the atlantoaxial joint, in addition to initial X-rays. All seven cervical vertebrae should be demonstrated on anteroposterior and lateral cervical spine X-rays.
Extremity trauma
The examination includes the following items.
Skin color and temperature, terminal arterial pulsation, location of abrasions and bleeding, presence of limb deformities, active and passive motion ;
paradoxical movements and bone rub sounds; pain plane reached by the injury.
Extremity injury management goals.
Ensure blood flow to distal tissues, prevent infection and skin necrosis, and prevent peripheral nerve injury.
Special points for extremity injuries.
Active bleeding should be stopped by direct pressure and no tourniquet should be used. This is because a tourniquet may be inadvertently forgotten to be released, which may cause ischemic damage.
Open fractures: Any injury in the vicinity of the fracture should be considered a contaminated injury. Principles of management include: hemostasis, bandaging, immobilization, and analgesia ;
Fascial compartment syndrome is a series of syndromes caused by increased pressure within the fascial space. The increased pressure within the fascial space can compress the blood vessels and peripheral nerves in the adjacent area. As a result of restricted blood perfusion and peripheral nerve damage, muscle ischemia and necrosis and functional limitation may eventually result.
(i) History of injury such as crushing of the affected limb, generalized swelling, and severe pain;
(ii) Increased limb tone and significant pressure pain;
③Muscle movement disorder;
④Passive muscle pulling pain in the limb;
⑤ Dysfunction of the nerve trunk of the limb, with sensory impairment preceding motor impairment.
The diagnosis can be confirmed by having the above three items ②, ③ and ④.
Early treatment: braking, no massage, no elevation of the affected limb
Treatment of the injured limb: early fasciotomy and decompression. Adequate decompression.
The consequences of fascial compartment syndrome are often underestimated and should be taken with a grain of salt.
Indications for decompression by incision: definite history; urine myoglobin (positive) or urine occult blood test (positive); involvement of more than one fascial compartment of the limb, blisters, and corresponding motor deficits.
Prevention of renal failure: correction of dehydration and shock; application of alkaline drugs: sodium bicarbonate is preferred; early application of diuretic drugs: mannitol, furosemide, etc. Sodium hesperidin: In addition to reducing tissue pressure, its anti-inflammatory effect is 7 times stronger than that of hydrocortisone.
Hypoxic tissue damage: Fascial compartment syndrome mostly has increased intramuscular pressure and poor local blood flow, commonly seen in trauma patients with intramuscular hematoma, stonewall contusion, fracture or amputation. If the perfusion pressure (systolic blood pressure) is low, a mild increase in intramuscular pressure can cause hypoperfusion. At normal body temperature, when systolic blood pressure is around 80 mmHg, limb blood flow and perfusion begin to decline.
The isolated limb should be wrapped in saline-wetted sterile gauze and stored in a sterile plastic bag. If not cryopreserved, the time limit for its use is 6 hours after the injury; if cryopreservation is done, the time limit can be extended to 18-20 hours after the injury.
Reperfusion injuries are often severe: if the local hypoxia time (high intramuscular pressure, low blood pressure) exceeds 2 hours, reperfusion can lead to extensive vascular damage. This is why early decompression should be performed. Fascial compartment syndrome of the forearm and lower extremities is particularly dangerous.
Burns
The priority management principles for burn patients are the same as for other trauma patients
Examination procedures: airway, respiration (note inhalation injury and rapidly deteriorating airway conditions), circulation (fluids), neurological examination (note the presence of fascial compartment syndrome), general examination (area of burn).
The source of the burn is important, such as fire, hot water, paraffin, kerosene, etc. Electrical burns are often more severe once they have occurred. Keep in mind that skin and muscle injuries can lead to acute renal failure.